Iptakalim inhibits PDGF-BB-induced human airway smooth muscle cells proliferation and migration

Liu, Wenrui; Kong, Hui; Zeng, Xianlu; Wang, Jingjing; Wang, Zailiang; Yan, Xiaopei; Wang, Yanli; Xie, Wei; Wang, Hong

doi:10.1016/j.yexcr.2015.06.020

Cited by 27 publications

(24 citation statements)

References 44 publications

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“…The present study revealed that PDGF-BB-induced ASM cell migration was partially mediated by inhibition of the activation of ERK and AKT. These data are consistent with those of previous studies in which the activation of ERK and AKT were demonstrated to mediate ASM proliferation and migration induced by various growth factors, including PDGF-BB (20,28,29). Furthermore, the present study revealed that the knockdown of FSTL1 markedly inhibited PDGF-BB-induced protein expression levels of p-ERK and p-AKT.…”

Section: Discussionsupporting

confidence: 93%

“…FSTL1 has been reported to inhibit proliferation and invasion, and to induce apoptosis of cancer cells in vitro (17,18). In addition, increasing evidence indicates that PDGF is involved in the pathophysiology of asthma, and that PDGF is a potent mitogen that may mediate ASM cell proliferation and migration (19)(20)(21). The present study revealed that knockdown of FSTL1 inhibited cell proliferation and arrested the cell cycle in the G2/M phase in PDGF-BB-stimulated ASM cells.…”

Section: Discussionsupporting

confidence: 52%

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Knockdown of FSTL1 inhibits PDGF-BB-induced human airway smooth muscle cell proliferation and migration

Deng

Zhang

et al. 2017

Molecular Medicine Reports

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Abnormal proliferation and migration of airway smooth muscle (ASM) cells serve roles in airway remodeling, and contribute to airway hyper‑responsiveness. Follistatin‑like protein 1 (FSTL1) is a secreted glycoprotein that belongs to the follistatin family of proteins. It was reported that in the lungs of patients suffering from severe asthma, FSTL1 is highly expressed by macrophages. However, the role of FSTL1 in ASM cell proliferation and migration remains unknown. The present study aimed to investigate the role of FSTL1 in cell proliferation and migration mediated by platelet‑derived growth factor subunit B (PDGF‑BB) in human ASM cells. The results of the present study demonstrated that PDGF‑BB stimulation upregulated FSTL1 expression levels in ASM cells in vitro. Knockdown of FSTL1 inhibited cell proliferation and arrested the cell cycle in the G2/M phase in PDGF‑BB‑stimulated ASM cells. Additionally, knockdown of FSTL1 inhibited PDGF‑BB‑induced ASM cell migration. Furthermore, FSTL1 knockdown caused the downregulation of phosphorylated (p)‑extracellular signal‑regulated kinase (ERK) and p‑protein kinase B (AKT) expression levels induced by PDGF‑BB in ASM cells. In conclusion, the present study demonstrated that knockdown of FSTL1 inhibited ASM cell proliferation and migration induced by PDGF‑BB, at least partially via inhibiting the activation of ERK and AKT. FSTL1 may therefore represent a novel therapeutic target for airway remodeling in childhood asthma.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 52%

Knockdown of FSTL1 inhibits PDGF-BB-induced human airway smooth muscle cell proliferation and migration

Deng

Zhang

et al. 2017

Molecular Medicine Reports

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“…All of the animals were purchased from the Animal Center of Southeast University. All of the animals were maintained under temperature-controlled (21-26°C) conditions, 40-70% humidity, and [15][16][17][18][19][20] Lux lighting with free access to water and food.…”

Section: Animalsmentioning

confidence: 99%

“…The proliferation of rat-VSMC was measured using the cell counting kit-8 (CCK-8) assay as previously reported [15].…”

Section: Cell Proliferation Assaymentioning

confidence: 99%

Kir2.1 regulates rat smooth muscle cell proliferation, migration, and post-injury carotid neointimal formation

Tang

Wang

et al. 2016

Biochemical and Biophysical Research Communications

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Phenotype switching of vascular smooth muscle cells (VSMC) from the contractile type to the synthetic type is a hallmark of vascular disorders such as atherosclerosis and restenosis after angioplasty. Inward rectifier K(+) channel 2.1 (Kir2.1) has been identified in VSMC. However, whether it plays a functional role in regulating cellular transformation remains obscure. In this study, we evaluated the role of Kir2.1 on VSMC proliferation, migration, phenotype switching, and post-injury carotid neointimal formation. Kir2.1 knockdown significantly suppressed platelet-derived growth factor BB-stimulated rat vascular smooth muscle cells (rat-VSMC) proliferation and migration. Deficiency in Kir2.1 contributed to the restoration of smooth muscle α-actin, smooth muscle 22α, and calponin and to a reduction in osteopontin expression in rat-VSMC. Moreover, the in vivo study showed that rat-VSMC switched to proliferative phenotypes and that knockdown of Kir2.1 significantly inhibited neointimal formation after rat carotid injury. Kir2.1 may be a potential therapeutic target in the treatment of cardiovascular diseases, such as atherosclerosis and restenosis following percutaneous coronary intervention.

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“…Western Blotting was performed as described previously [5]. Equal amount of total protein was loaded on 12% sodium dodecylsulfate polyacrylamide gel.…”

Section: Wesltern Blottingmentioning

confidence: 99%

The Role of Myocardin in Platelet-derived Growth Factor-BB-induced Phenotypic Switching of Vascular Smooth Muscle Cells

Song¹,

Wang²,

Huang³

et al. 2016

Proceedings of the 2016 2nd International Conference on Architectural, Civil and Hydraulics Engineering (ICACHE 2016)

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Abstract. In recent years, numerous studies confirm that platelet-derived growth factor-BB (PDGF-BB) is involved in the development of atherosclerosis and the regulation of human aorta VSMC (HA-VSMC) proliferation. Myocardin is an essential transcription factor that can activate the transcription of some smooth muscle marker genes. Our results showed that HA-VSMCs treated with PDGF-BB exhibited morphological changes from spindle-shaped to polygonal shape. The expression of proliferation marker gene CyclinD1, osteopontin (OPN), proliferating cell nuclear antigen (PCNA) were increased in PDGF-BB-treated HA-VSMCs. 5-ethynyl-2′-deoxyuridine incorporation assay (EdU) and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay confirmed that cell viability and proliferative ability were increased significantly in PDGF-BB treated HA-SMCs. Next, the expression of transcription factor myocardin was decreased in PDGF-BBtreated HA-VSMCs. These results preliminarily demonstrated the role of myocardin in phenotypic switching of PDGF-BB-induced HA-VSMCs.

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Iptakalim inhibits PDGF-BB-induced human airway smooth muscle cells proliferation and migration

Cited by 27 publications

References 44 publications

Knockdown of FSTL1 inhibits PDGF-BB-induced human airway smooth muscle cell proliferation and migration

Knockdown of FSTL1 inhibits PDGF-BB-induced human airway smooth muscle cell proliferation and migration

Kir2.1 regulates rat smooth muscle cell proliferation, migration, and post-injury carotid neointimal formation

The Role of Myocardin in Platelet-derived Growth Factor-BB-induced Phenotypic Switching of Vascular Smooth Muscle Cells

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